Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.1.2.42 (DTA)
1,693 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Comparative study of ionic and nonionic contrast media was carried out to investigate the effects on the cardiac conducting system caused by sodium ion and osmolality in coronary angiography. We evaluated the effects on the cardiac conducting system by 5% Glucose (5% GL), 20% glucose (20% GL), saline (SL), Ioxaglate 320 (IOX, ionic low-osmolar contrast medium, ionic LOCM), Iopamidol 370 (IOP 370, non ionic low-osmolar contrast medium, nonionic LOM) and 60% Diatrizoate (DTA, high-osmolar contrast medium, HOCM). In 18 patients who underwent coronary angiography, the effects on the cardiac conducting system were investigated using P-P time, A-H time, H-V time, QTc, T-wave height from His bundle electrogram and surface electrocardiogram. Prolongations of P-P time, A-H time and QTc with 20% GL, DTA were significantly longer than with IOX, IOP 370, 5% GL, and SL (p less than 0.01). There was almost no difference among 5% GL, SL, IOX, and IOP 370 in both P-P and A-H times. Also, prolongations of QTc with IOX, IOP 370 were longer than with 5% GL and SL (p less than 0.01). H-V time was not significantly prolonged with all solutions. The change of T-wave height with IOX was significantly greater than with IOP 370 (p less than 0.01). The change of T-wave height with SL was significantly greater than with 5% GL and that of T-wave height with 60% DTA was significantly greater than with 20% GL (p less than 0.01). Prolongations of P-P time, A-H time, QTc and changes of T-wave height were correlated with osmolality (p less than 0.01). These observations suggested that main factor of the disturbances of the cardiac conducting system excluding change of T-wave height was high osmolality of solution. Sodium ion took little part in the disturbances, and the factor of T-wave height change was not only due to the osmolality but also due to the concentration of sodium ion. LOCM caused much less significant disturbances of the cardiac conducting system than HOCM. There was almost no difference between non-ionic LOCM and ionic LOCM excluding the change of T-wave height.
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PMID:[The effects of contrast media on the cardiac conducting system in coronary angiography]. 260

Analysis of blood of fasted rats revealed two endogenous sugar acids, 3,4-dihydroxybutanoic acid (2-deoxytetronic acid; 2-DTA) and 2,4,5-trihydroxypentanoic acid (3-deoxypentonic acid; 3-DPA), that might be related to food intake control. Injection of 2-DTA into the third cerebral ventricle reduced food intake for 24 hr in 72 hr deprived rats and depressed single neurons activity in the lateral hypothalamus (LHA). The same amounts of 3-DPA elicited feeding in a dose-related fashion, and increased LHA single neuron activity with 6 to 8 min latency. Intravenous injection of 3-DPA, but not 2-DTA, was effective. Liposome encapsulation of 2-DTA enhanced its potency after intraperitoneal injection, probably by allowing passage across the blood-brain barrier. Electrophoretic application of 2-DTA significantly and specifically suppressed, and 3-DPA facilitated activity of glucose-sensitive (GS) neurons in the LHA. Neither affected glucose insensitive LHA neurons. Both sugar acids affected glucoreceptor (GR) neuron activity oppositely in the ventromedial hypothalamic nucleus (VMH). Intracellular recordings verified that the effect of 2-DTA on the GS and GR neurons was the same as glucose. Hyperpolarization of GR neurons with a membrane conductance increase was brought about by 3-DPA. The levels of plasma glucose and insulin changed oppositely by 2-DTA and 3-DPA, respectively when these were applied into the third cerebral ventricle. Feeding behavior and LHA and VMH neuron activity changes after injection suggest 2-DTA may be an endogenous satiety substance and 3-DPA a hunger substance, with effects mediated by GS neurons in LHA and GR neurons in VMH. Effects of 3-hydroxybutyric acid were also verified and discussed.
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PMID:Feeding regulation by endogenous sugar acids through hypothalamic chemosensitive neurons. 353 1

Hypophagia induced by 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA), an endogenous short-chain polyhydroxymonocarboxylic acid, was investigated in rats. Intraperitoneal injection of 2500 mumol 2-DTA did not suppress feeding, but 2.5 mumol 2-DTA injected into the third cerebroventricle did. To efficiently transport exogenous 2-DTA into the brain, its encapsulation and delivery in specially made sulfatide liposomes was attempted. Feeding was suppressed dose-dependently by intraperitoneally injected 2-DTA in liposomes. Injection of 2500 mumol 2-DTA into the common carotid artery also suppressed feeding. Administration by either route prolonged postprandial intermeal interval with no change in meal size, as was observed after central administration of 2-DTA. Injection of 2.5 mumol 2-DTA into the third cerebroventricle elevated plasma glucose level, leaving insulin and free fatty acids unaffected. These findings, together with previous results, indicate that at least one site for the physiological action of 2-DTA is in the hypothalamic centers for food intake.
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PMID:Hypophagia induced by endogenous or liposome-encapsulated 3,4-dihydroxybutanoic acid. 354 29

The feeding related endogenous sugar acids, 2-deoxytetronic acid, 2-DTA and 3-deoxypentonic acid, 3-DPA, were investigated for their peripheral and central (hypothalamic) control of gastric acid secretion, and effects on activity of lateral hypothalamic (LHA) neurons in rats. Peripheral gastric acid secretion was not affected by either 2-DTA or 3-DPA. Slight gastric acid secretion was elicited by 3-DPA only when it was applied directly into the gastric related site of the LHA. Gastric acid secretion induced by 2-deoxy-D-glucose (2DG) was suppressed by application of 2-DTA in the LHA. 3-DPA had no effect on 2DG induced secretion. Electrophoretic application of 2-DTA significantly inhibited the activity of both gastric and non-gastric type glucose-sensitive neurons in the LHA, and 3-DPA significantly excited both types of glucose-sensitive neurons. The results agree with previous reports that 2-DTA and 3-DPA are endogenous satiety and hunger factors, respectively, and act by modulating hypothalamic control of gastric acid secretion which is mediated through gastric type and non-gastric type glucose-sensitive neurons.
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PMID:Endogenous sugar acid control of hypothalamic neuron activity and gastric acid secretion in rats. 402 89

Endogenous sugar acids, 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA) and 2,4,5-trihydroxypentanoic acid (3-deoxypentonic acid, 3-DPA), have been identified in the serum of fasted rats. Effects of these sugar acids on rat feeding behavior and neuron activity were investigated. Injections of 2-DTA (2.5 mumol) into the third cerebral ventricle of chronic rats suppressed food intake and single-neuron activity in the lateral hypothalamic area (LHA). Food consumption was reduced for 24 h, even in 72-h food-deprived rats. The same amounts of 3-DPA elicited feeding and increased LHA single-neuron activity with latencies of 6-8 min. Electrophoretically applied 2-DTA significantly and specifically suppressed activity of glucose-sensitive neurons in the LHA, whereas 3-DPA facilitated the activity. Nonglucose-sensitive LHA neurons were not affected by these sugar acids. The high correlation between modulation of feeding behavior and changes in LHA neuron activity after injection of these sugar acids suggested that 2-DTA may act as an endogenous satiety substance and 3-DPA as a hunger substance. The effects may be mediated through glucose-sensitive neurons in the LHA.
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PMID:Modulation of feeding by endogenous sugar acids acting as hunger or satiety factors. 672 Sep 28

We have investigated the antidiabetic action of troglitazone in aP2/DTA mice, whose white and brown fat was virtually eliminated by fat-specific expression of diphtheria toxin A chain. aP2/DTA mice had markedly suppressed serum leptin levels and were hyperphagic, but did not gain excess weight. aP2/DTA mice fed a control diet were hyperlipidemic, hyperglycemic, and had hyperinsulinemia indicative of insulin-resistant diabetes. Treatment with troglitazone alleviated the hyperglycemia, normalized the tolerance to intraperitoneally injected glucose, and significantly decreased elevated insulin levels. Troglitazone also markedly decreased the serum levels of cholesterol, triglycerides, and free fatty acids both in wild-type and aP2/DTA mice. The decrease in serum triglycerides in aP2/DTA mice was due to a marked reduction in VLDL- and LDL-associated triglyceride. In skeletal muscle, triglyceride levels were decreased in aP2/DTA mice compared with controls, but glycogen levels were increased. Troglitazone treatment decreased skeletal muscle, but not hepatic triglyceride and increased hepatic and muscle glycogen content in wild-type mice. Troglitazone decreased muscle glycogen content in aP2/DTA mice without affecting muscle triglyceride levels. The levels of peroxisomal proliferator-activated receptor gamma mRNA in liver increased slightly in aP2/DTA mice and were not changed by troglitazone treatment. The results demonstrate that insulin resistance and diabetes can occur in animals without significant adipose deposits. Furthermore, troglitazone can alter glucose and lipid metabolism independent of its effects on adipose tissue.
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PMID:Troglitazone action is independent of adipose tissue. 938 57

Brown adipose tissue (BAT) has the capacity for uncoupled mitochondrial respiration and is proposed to be a key site for regulating energy expenditure in rodents. To better define the role of BAT in energy homeostasis, we previously created a line of transgenic mice with deficiency of BAT (UCP promoter-driven diphtheria toxin A transgenic mice [UCP-DTA]) mice. These mice develop obesity that initially is due to decreased energy expenditure and later accompanied by hyperphagia despite increased levels of circulating leptin. In addition, the obesity of these mice is accompanied by severe insulin-resistant diabetes and hyperlipidemia. To better define the basis for leptin resistance in this model, we treated UCP-DTA mice with leptin (300 microg i.p., b.i.d.) and compared their response with that of leptin-treated ob/ob and FVB control mice (30 microg i.p., b.i.d.). Leptin treatment of FVB and ob/ob mice decreased their body weight and food intake and improved their glucose homeostasis. In contrast, tenfold higher dosages of leptin had no effect on body weight, food intake, or circulating insulin or glucose concentrations of UCP-DTA mice. Hypothalamic neuropeptide Y (NPY) mRNA expression was lower in UCP-DTA mice than in littermate control FVB mice in the fed state, and increased progressively in response to food restriction as leptin levels fell. In parallel to the levels of hypothalamic NPY, corticosterone levels were initially suppressed and rose with food restriction. Thus food intake, body weight, and insulin and glucose homeostasis of UCP-DTA mice are all extraordinarily resistant to leptin, whereas hypothalamic NPY and the hypothalamopituitary adrenal (HPA) axis may remain under leptin control. Further elucidation of the mechanisms underlying leptin resistance in UCP-DTA mice may provide valuable insights into the basis for leptin resistance in human obesity.
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PMID:Severe leptin resistance in brown fat-deficient uncoupling protein promoter-driven diphtheria toxin A mice despite suppression of hypothalamic neuropeptide Y and circulating corticosterone concentrations. 951 18

Ciliary neurotrophic factor (CNTF) potently reduces appetite and body weight in rodents and humans. We studied the short- and long-term effects of CNTF(Ax15), a second-generation CNTF analog, in diet-induced obese C57BL/6J mice and brown adipose tissue (BAT)-deficient obese UCP1-DTA (uncoupling protein 1-diphtheria toxin A) mice. CNTF(Ax15) administration (0.1, 0.3, or 1.0 microg . g(-1) . day(-1) s.c.) for 3 or 7 days reduced food intake and body weight (mainly body fat mass). The effect of CNTF(Ax15) on food intake and body weight was more pronounced in CNTF(Ax15)-treated diet-induced obese C57BL/6J mice compared with pair-fed controls and was associated with suppressed expression of hypothalamic neuropeptide Y and agouti gene-related protein. Moreover, CNTF(Ax15) increased uncoupling protein 1 mRNA expression in BAT and energy expenditure in diet-induced obese C57BL/6J mice. Longitudinal observations revealed a sustained reduction in body weight for several days post-CNTF(Ax15) treatment of CNTF(Ax15)-treated but not pair-fed mice, followed by a gradual regain in body weight over 28 days. Finally, CNTF(Ax15) administration improved the metabolic profile in both diet-induced obese C57BL/6J and UCP1-DTA mice and resulted in a significantly improved glycemic response to oral glucose tolerance tests in CNTF(Ax15)-treated UCP1-DTA compared with pair-fed mice of similar body weight. These data suggest that CNTF(Ax15) may act through a pathway downstream of the putative point responsible for leptin resistance in diet-induced obese C57BL/6J and UCP1-DTA mice to alter food intake, body weight, body composition, and metabolism. CNTF(Ax15) has delayed and persistent effects in diet-induced obese C57BL/6J mice, which account for a reduction in body weight over and above what would be expected based on decreased foot intake alone.
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PMID:Ciliary neurotrophic factorAx15 alters energy homeostasis, decreases body weight, and improves metabolic control in diet-induced obese and UCP1-DTA mice. 1550 58

Resistin is an adipocyte-secreted hormone proposed to link obesity with insulin resistance and diabetes, but no previous study has performed a joint quantitative evaluation of white adipose tissue (WAT) resistin mRNA expression and serum levels in relation to insulinemia and glycemia in mice. We have thus comparatively assessed WAT resistin mRNA expression and serum resistin levels in lean C57BL/6J mice and various mouse models of obesity, including diet-induced obese (DIO) C57BL/6J mice, high fat-fed TNF-alpha-/- mice, and brown adipose tissue (BAT)-deficient uncoupling protein-diphtheria toxin A chain (UCP1-DTA) mice. We also studied whether treatment with the weight-reducing and insulin-sensitizing compounds, MTII, an alpha-melanocyte-stimulating hormone analog, or CNTF(Ax15), a ciliary neurotrophic factor analog, alters resistin mRNA expression and/or circulating levels in lean and DIO C57BL/6J mice. We find that resistin mRNA expression is similar in DIO and lean C57BL/6J mice, as well as in TNF-alpha-/- and wild-type (WT) mice. Circulating resistin levels, however, are higher in DIO C57BL/6J, high fat-fed TNF-alpha-/-, and UCP1-DTA mice compared with lean controls. Moreover, although resistin mRNA expression is upregulated by MTII treatment for 24 h and downregulated by CNTF(Ax15) treatment for 3 or 7 days, circulating resistin levels are not altered by MTII or CNTF(Ax15) treatment. In addition, serum resistin levels, but not resistin mRNA expression levels, are correlated with body weight, and neither resistin mRNA expression nor serum resistin levels are correlated with serum insulin or glucose levels. We conclude that transcriptional regulation of resistin in WAT does not correlate with circulating resistin levels and that circulating resistin is unlikely to play a major endocrine role in insulin resistance or glycemia in mice.
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PMID:Circulating resistin in lean, obese, and insulin-resistant mouse models: lack of association with insulinemia and glycemia. 1552 96

A variety of bacterial strains were isolated from waste disposal sites of Uttaranchal, India, and some from artificially developed soil beds containing maleic anhydride, glucose, and small pieces of polyethylene. Primary screening of isolates was done based on their ability to utilize high- and low-density polyethylenes (HDPE/LDPE) as a primary carbon source. Thereafter, a consortium was developed using potential strains. Furthermore, a biodegradation assay was carried out in 500-ml flasks containing minimal broth (250 ml) and HDPE/ LDPE at 5 mg/ml concentration. After incubation for two weeks, degraded samples were recovered through filtration and subsequent evaporation. Fourier transform infrared spectroscopy (FTIR) and simultaneous thermogravimetric-differential thermogravimetry-differential thermal analysis TG-DTG-DTA) were used to analyze these samples. Results showed that consortium-treated HDPE (considered to be more inert relative to LDPE) was degraded to a greater extent 22.41% weight loss) in comparison with LDPE (21.70% weight loss), whereas, in the case of untreated samples, weight loss was more for LDPE than HDPE (4.5% and 2.5%, respectively) at 400 degrees . Therefore, this study suggests that polyethylene could be degraded by utilizing microbial consortia in an eco-friendly manner.
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PMID:Comparative biodegradation of HDPE and LDPE using an indigenously developed microbial consortium. 1838 65


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